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3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165770 | GEO | 2024/01/01

REPOSITORIES: GEO

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3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α.

Project description:The human ζ-globin gene (HBZ) is transcribed in primitive erythroid cells only during the embryonic stages of development. Reactivation of this embryonic globin synthesis would likely alleviate symptoms both in α-thalassemia and sickle-cell disease. However, the molecular mechanisms controlling ζ-globin expression have remained largely undefined. Moreover, the pharmacologic agent capable of inducing ζ-globin production is currently unavailable. Here, we show that TRIAC, a bioactive thyroid hormone metabolite, significantly induced ζ-globin gene expression during zebrafish embryogenesis. The induction of ζ-globin expression by TRIAC was also observed in human K562 erythroleukemia cell line and primary erythroid cells. Thyroid hormone receptor α (THRA) deficiency abolished the ζ-globin-inducing effect of TRIAC. Furthermore, THRA could directly bind to the distal enhancer regulatory element to regulate ζ-globin expression. Our study provides the first evidence that TRIAC acts as a potent inducer of ζ-globin expression, which might serve as a new potential therapeutic option for patients with severe α-thalassemia or sickle-cell disease.

| S-EPMC8235803 | biostudies-literature

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α.

| S-EPMC8235803 | biostudies-literature

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (RNA-seq)

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of K562 cells treated with DMSO and TRIAC

2024-01-01 | GSE165769 | GEO

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (ChIP-seq)

Project description:To characterize genome-wide THRA traget genes in K562 cells.

2024-01-01 | GSE165768 | GEO

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

Project description:3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

| PRJNA697855 | ENA

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (ChIP-seq)

Project description:3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (ChIP-seq)

| PRJNA697859 | ENA

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (RNA-seq)

Project description:3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (RNA-seq)

| PRJNA697860 | ENA

Thyroid hormone induces cerebellar Purkinje cell dendritic development via the thyroid hormone receptor alpha1.

Project description:The thyroid hormone l-3,3',5-triiodothyronine (T3) plays an important role during cerebellar development. Perinatal T3 deficiency leads to severe cellular perturbations, among them a striking reduction in the growth and branching of Purkinje cell dendritic arborization. The molecular mechanisms underlying these effects are poorly understood. Despite the well documented broad expression of thyroid hormone receptors (TRs), analysis of different TR-deficient mice has failed to provide detailed information about the function of distinct TRs during neuronal development. The cerebellar cell culture systems offer an excellent model by which to study the effects of T3, because differentiation of cerebellar neurons in mixed and purified cultures proceeds in the absence of serum that contains T3. Addition of T3 to cerebellar cultures causes a dramatic increase in Purkinje cell dendrite branching and caliber in a dose- and time-dependent manner. Furthermore, we demonstrate for the first time that T3 acts on Purkinje cells directly through TRalpha1 expressed on the Purkinje cell and not on the granule cell, the presynaptic partner of Purkinje cells. In contrast, TRbeta isoforms are not involved, because Purkinje cells derived from TRbeta-/- mice show the same T3 responsiveness as wild-type cells. T3-promoted Purkinje cell differentiation was not mediated via neurotrophins, as suggested previously, because dendritogenesis of Purkinje cells from BDNF-/- mice could be effectively stimulated in vitro by T3 treatment. Furthermore, the effects of T3 observed were not abolished by tyrosine kinase receptor B (TrkB)-IgG, TrkC-IgG, or K252a, agents known to block the actions of neurotrophin. These results indicate that T3 directly affects Purkinje cell differentiation through activation of the TRalpha1.

| S-EPMC6740935 | biostudies-literature

Increased sensitivity to thyroid hormone in mice with complete deficiency of thyroid hormone receptor alpha.

Project description:Only three of the four thyroid hormone receptor (TR) isoforms, alpha1, beta1, and beta2, bind thyroid hormone (TH) and are considered to be true TRs. TRalpha2 binds to TH response elements on DNA, but its role in vivo is still unknown. We produced mice completely deficient in TRalpha (TRalpha(o/o)) that maintain normal serum thyroid-stimulating hormone (TSH) concentration despite low serum thyroxine (T(4)), suggesting increased sensitivity to TH. We therefore examined the effects of TH (L-3,3',5-triiodothyronine, L-T3) given to TH-deprived and to intact TRalpha(o/o) mice. Controls were wild-type (WT) mice of the same strain and mice resistant to TH due to deficiency in TRbeta (TRbeta(-/-)). In liver, T3 produced significantly greater responses in TRalpha(o/o) and smaller responses in TRbeta(-/-) as compared with WT mice. In contrast, cardiac responses to L-T3 were absent or reduced in TRalpha(o/o), whereas they were similar in WT and TRbeta(-/-) mice, supporting the notion that TRalpha1 is the dominant TH-dependent TR isoform in heart. 5-Triiodothyronine (L-T3) given to intact mice produced a greater suppression of serum T(4) in TRalpha(o/o) than it did in WT mice and reduced by a greater amount the TSH response to TSH-releasing hormone. This is an in vivo demonstration that a TR deficiency can enhance sensitivity to TH. This effect is likely due to the abrogation of the constitutive "silencing" effect of TRalpha2 in tissues expressing the TRbeta isoforms.

| S-EPMC14593 | biostudies-literature

Thyroid Hormone Receptor Alpha Is Required for Thyroid Hormone-Dependent Neural Cell Proliferation During Tadpole Metamorphosis.

Project description:Thyroid hormone (T3) plays several key roles in development of the nervous system in vertebrates, controlling diverse processes such as neurogenesis, cell migration, apoptosis, differentiation, and maturation. In anuran amphibians, the hormone exerts its actions on the tadpole brain during metamorphosis, a developmental period dependent on T3. Thyroid hormone regulates gene transcription by binding to two nuclear receptors, TRα and TRβ. Our previous findings using pharmacological and other approaches supported that TRα plays a pivotal role in mediating T3 actions on neural cell proliferation in Xenopus tadpole brain. Here we used Xenopus tropicalis (X. tropicalis) tadpoles with an inactivating mutation in the gene that encodes TRα to investigate roles for TRα in mitosis and gene regulation in tadpole brain. Gross morphological analysis showed that mutant tadpoles had proportionally smaller brains, corrected for body size, compared with wildtype, both during prometamorphosis and at the completion of metamorphosis. This was reflected in a large reduction in phosphorylated histone 3 (pH3; a mitosis marker) immunoreactive (ir) nuclei in prometamorphic tadpole brain, when T3-dependent cell proliferation is maximal. Treatment of wild type premetamorphic tadpoles with T3 for 48 h induced gross morphological changes in the brain, and strongly increased pH3-ir, but had no effect in mutant tadpoles. Thyroid hormone induction of the direct TR target genes thrb, klf9, and thibz was dysregulated in mutant tadpoles. Analysis of gene expression by RNA sequencing in the brain of premetamorphic tadpoles treated with or without T3 for 16 h showed that the TRα accounts for 95% of the gene regulation responses to T3.

| S-EPMC6610206 | biostudies-literature

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